Posts tagged brain
Articles and news from the latest research reports.
Diabetes Raises Levels of Proteins Linked to Alzheimer’s Features
Growing evidence suggests that there may be a link between diabetes and Alzheimer’s disease, but the physiological mechanisms by which diabetes impacts brain function and cognition are not fully understood. In a new study published in Aging Cell, researchers at the Salk Institute for Biological Studies show, for the first time, that diabetes enhances the development of aging features that may underlie early pathological events in Alzheimer’s.
Specifically, the Salk team found increases in two hallmarks of Alzheimer’s-accumulations of amyloid beta (Abeta) and tau protein-in the brains of diabetic mice, especially in cells surrounding blood vessels. Abeta, the misfolded peptide that is thought in part to cause Alzheimer’s disease, aggregated inside astrocytes, star-shaped brain cells that, upon interaction with Abeta, release inflammatory molecules that can destroy neurons. Previously, this had not been shown in mouse models of type 1 diabetes (T1D).
"Our study supports and extends the links between diabetes, aging and Alzheimer’s," says senior author Pamela Maher, a senior staff scientist in Salk’s Laboratory of Cellular Neurobiology. "We show that type 1 diabetes increases vascular-associated amyloid beta buildup in the brain and causes accelerated brain aging."
The findings suggest that the neurovascular system may be a good candidate for new therapeutic targets to treat Alzheimer’s in the early stages of the disease.
Magnetic brain stimulation treats depression independent of sleep effect
While powerful magnetic stimulation of the frontal lobe of the brain can alleviate symptoms of depression, those receiving the treatment did not report effects on sleep or arousal commonly seen with antidepressant medications, researchers say.
“People’s sleep gets better as their depression improves, but the treatment doesn’t itself cause sedation or insomnia.” said Dr. Peter B. Rosenquist, Vice Chair of the Department of Psychiatry and Health Behavior at the Medical College of Georgia at Georgia Health Sciences University.
The finding resulted from a secondary analysis of a study of 301 patients at 23 sites comparing the anti-depressive effects of the Neuronetics Transcranial Magnetic Stimulation Therapy System to sham (placebo) treatment in patients resistant to antidepressant medications. TMS sessions were given for 40 minutes, five days a week for six weeks. Initial findings, published in the journal Biological Psychiatry in 2007, were the primary evidence in the Food and Drug Administration’s approval of TMS for depression. The secondary review reaffirmed TMS’s effectiveness in depression but revealed no differences in rates of insomnia or sleepiness among those who got actual and sham (placebo) therapy. Patients in the treatment group were also no more likely to request medication for insomnia or anxiety.
“It’s important for us to understand the full range of the effects of any treatment we give,” said Rosenquist, corresponding author of the study in the journal Psychiatric Research. The new findings will assuage worries of sleep-related side effects and remind physicians to remain alert to residual insomnia in depressed patients they are treating with TMS, the researchers report.
Sleep problems are a common side effect of major antidepressants: some drugs sedate patients while others stimulate them and increase insomnia. Insomnia occurs in 50-90 percent of patients with major depressive disorder. Other depressed patients complain they sleep too much. The good news is that TMS does not contribute to insomnia or oversleeping.
“One of the many bad things about depression is that often patients cannot sleep. We think it’s a significant symptom,” Rosenquist said. “If patients can’t sleep, it really adds to their distress, and even increases the likelihood of suicide. We need antidepressant treatments that patients can tolerate so that they will stay with the treatment, which takes weeks to fully achieve. Our study adds to the evidence showing that TMS has remarkably few side effects.” Patients often seek TMS as an option or adjunct to medication to avoid medication side effects.
“Mood disorders are associated with widespread structural and functional changes in the human brain, which can be reversed with successful treatment,” Rosenquist said. “Clinical researchers are working to find the optimal way to restore normal brain function.”
TMS targets the prefrontal cortex of the brain, involved in mood regulation as well as other higher-order functions like planning, evaluating and decision-making. In this procedure, patients sit in a recliner and receive brief pulses of a MRI strength magnet held against the front of the head. The magnetic energy of TMS causes the brain cells closest to the surface of the brain to increase their activity which in turn influences the activity of the brain as a whole.
Major Depressive Disorder affects approximately 14.8 million, or about 6.7 percent of American adults in a given year, according to the National Institute of Mental Health. It’s the leading cause of disability in ages 15 to 44. Despite the numbers, Rosenquist concedes that it’s not clear what causes depression or exactly how antidepressants and other therapies, such as TMS, work. “It’s an important puzzle and the work continues. We are excited to be a part of this effort at Georgia Health Sciences University.”
(Source: news.georgiahealth.edu)
New clues to how the brain and body communicate to regulate weight
Maintaining a healthy body weight may be difficult for many people, but it’s reassuring to know that our brains and bodies are wired to work together to do just that—in essence, to achieve a phenomenon known as energy balance, a tight matching between the number of calories consumed versus those expended. This careful balance results from a complex interchange of neurobiological crosstalk within regions of the brain’s hypothalamus, and when this “conversation” goes awry, obesity or anorexia can result.
Given the seriousness of these conditions, it’s unfortunate that little is known about the details of this complex interchange. Now research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) provides new insights that help bring order to this complexity. Described in the October 26 issue of the journal Cell, the findings demonstrate how the GABA neurotransmitter selectively drives energy expenditure, and importantly, also help explain the neurocircuitry underlying the fat-burning properties of brown fat.
"Our group has built up a research program with the overall goal of unraveling the ‘wiring diagram’ by which the brain controls appetite and the burning of calories," says senior author Bradford Lowell, MD, PhD, a Professor of Medicine in BIDMC’s Division of Endocrinology and Harvard Medical School. "To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable."
Omega-3 Intake Heightens Working Memory in Healthy Young Adults
While Omega-3 essential fatty acids—found in foods like wild fish and grass-fed livestock—are necessary for human body functioning, their effects on the working memory of healthy young adults have not been studied until now.
In the first study of its kind, researchers at the University of Pittsburgh have determined that healthy young adults ages 18-25 can improve their working memory even further by increasing their Omega-3 fatty acid intake. Their findings have been published online in PLOS One.
“Before seeing this data, I would have said it was impossible to move young healthy individuals above their cognitive best,” said Bita Moghaddam, project investigator and professor of neuroscience. “We found that members of this population can enhance their working memory performance even further, despite their already being at the top of their cognitive game.”
(Image credit: Matt Allworth/Courtesy Flickr)
Same neurons at work in sleep and under anesthesia
Anesthesiologists aren’t totally lying when they say they’re going to put you to sleep. Some anesthetics directly tap into sleep-promoting neurons in the brain, a study in mice reveals.
The results may help clarify how drugs that have been used around the world for decades actually put someone under. “It’s kind of shocking that after 170 years, we still don’t understand why they work,” says study coauthor Max Kelz of the University of Pennsylvania in Philadelphia.
Most neurons in the brain appear to be calmed by anesthetics, says neuropharmacologist and anesthesiologist Hugh Hemmings Jr. of Weill Cornell Medical College in New York City. But the new results, published online October 25 in Current Biology, show that two common anesthetics actually stimulate sleep-inducing neurons. “It’s unusual for neurons to be excited by anesthetics,” Hemmings says.
In the study, Kelz, Jason Moore, also of the University of Pennsylvania, and colleagues studied the effects of the anesthetics isoflurane and halothane. Mice given the drugs soon became sleepy, as expected. Along with this drowsiness came a jump in nerve cell activity in a part of the brain’s hypothalamus called the ventrolateral preoptic nucleus, or VLPO.
Speed-Learning a New Language May Help Brain Grow
Learning a new language over a short period of time appears to make the brain grow, new research suggests. The new study included young recruits at the Swedish Armed Forces Interpreter Academy who went from having no knowledge of a new language to speaking it fluently within 13 months. The recruits studied at a furious pace: from morning to evening, weekdays and weekends.
The recruits were compared to medicine and cognitive science students at a university (the “control” group), who also studied hard, but weren’t learning a new language. Both groups underwent MRI brain scans before and after a three-month period of intensive study. The scans showed that the brain structure of the control group remained unchanged, but certain parts of the brain of the language students grew.
This growth occurred in the hippocampus, a structure involved in learning new material and spatial navigation, and in three areas of the cerebral cortex. Among the recruits, those who took naturally to learning a new language had greater growth in the hippocampus and areas of the cerebral cortex related to language learning, while those who had to put more effort into learning a new language had greater growth in an area of the motor region of the cerebral cortex, the investigators found.
"We were surprised that different parts of the brain developed to different degrees depending on how well the students performed and how much effort they had had to put in to keep up with the course," Johan Martensson, a researcher in psychology at Lund University in Sweden, said in a university news release.
Martensson noted that previous research has indicated that bilingual and multilingual people develop Alzheimer’s disease at a later age. “Even if we cannot compare three months of intensive language study with a lifetime of being bilingual, there is a lot to suggest that learning languages is a good way to keep the brain in shape,” Martensson said.
The study appeared in the Oct. 15 issue of the journal NeuroImage.
Loneliness? It’s all a state of mind
Researchers from UCL have found that lonely people have less grey matter in a part of the brain associated with decoding eye gaze and other social cues.
Published in the journal of Current Biology, the study also suggests that through training people might be able to improve their social perception and become less lonely.
“What we’ve found is the neurobiological basis for loneliness,” said lead author Dr Ryota Kanai (UCL Institute of Cognitive Neuroscience). “Before conducting the research we might have expected to find a link between lonely people and the part of the brain related to emotions and anxiety, but instead we found a link between loneliness and the amount of grey matter in the part of the brain involved in basic social perception.”
To see how differences in loneliness might be reflected in the structure of the brain regions associated with social processes, the team scanned the brains of 108 healthy adults and gave them a number of different tests. Loneliness was self-reported and measured using a UCLA loneliness scale questionnaire.
When looking at full brain scans they saw that lonely individuals have less greymatter in the left posterior superior temporal sulcus (pSTS)—an area implicated in basic social perception, confirming that loneliness was associated with difficulty in processing social cues.
“The pSTS plays a really important role in social perception, as it’s the initial step of understanding other people,” said Dr Kanai. “Therefore the fact that lonely people have less grey matter in their pSTS is likely to be the reason why they have poorer perception skills.”
In order to gauge social perception, participants were presented with three different faces on a screen and asked to judge which face had misaligned eyes and whether they were looking either right or left. Lonely people found it much harder to identify which way the eyes were looking, confirming the link between loneliness, the size of the pSTS and the perception of eye gaze.
“From the study we can’t tell if loneliness is something hardwired or environmental,” said co-author Dr Bahador Bahrami (UCL Institute of Cognitive Neuroscience). “But one possibility is that people who are poor at reading social cues may experience difficulty in developing social relationships, leading to social isolation and loneliness.”
One way to counter this loneliness could be through social perception training with a smartphone app.
“The idea of training is one way to address this issue, as by maybe using a smartphone app to improve people’s basic social perception such as eye gaze, hopefully we can help them to lead less lonely lives,” said Dr Kanai.
(Source: ucl.ac.uk)
Rutgers Researchers Say Daily Drinking Can Be Risky
Study finds moderate consumption decreases number of new brain cells
Drinking a couple of glasses of wine each day has generally been considered a good way to promote cardiovascular and brain health. But a new Rutgers University study indicates that there is a fine line between moderate and binge drinking – a risky behavior that can decrease the making of adult brain cells by as much as 40 percent.
In a study posted online and scheduled to be published in the journal Neuroscience on November 8, lead author Megan Anderson, a graduate student working with Tracey J. Shors, Professor II in Behavioral and Systems Neuroscience in the Department of Psychology, reported that moderate to binge drinking – drinking less during the week and more on the weekends – significantly reduces the structural integrity of the adult brain.
“Moderate drinking can become binge drinking without the person realizing it,” said Anderson.“In the short term there may not be any noticeable motor skills or overall functioning problems, but in the long term this type of behavior could have an adverse effect on learning and memory.”
(Source: news.rutgers.edu)
Parkinson’s breakthough could slow disease progression
In an early-stage breakthrough, a team of Northwestern University scientists has developed a new family of compounds that could slow the progression of Parkinson’s disease.
Parkinson’s, the second most common neurodegenerative disease, is caused by the death of dopamine neurons, resulting in tremors, rigidity and difficulty moving. Current treatments target the symptoms but do not slow the progression of the disease.
The new compounds were developed by Richard B. Silverman, the John Evans Professor of Chemistry at the Weinberg College of Arts and Sciences and inventor of the molecule that became the well-known drug Lyrica, and D. James Surmeier, chair of physiology at Northwestern University Feinberg School of Medicine. Their research was published Oct. 23 in the journal Nature Communications.
The compounds work by slamming the door on an unwelcome and destructive guest — calcium. The compounds target and shut a relatively rare membrane protein that allows calcium to flood into dopamine neurons. Surmeier’s previously published research showed that calcium entry through this protein stresses dopamine neurons, potentially leading to premature aging and death. He also identified the precise protein involved — the Cav1.3 channel.
"These are the first compounds to selectively target this channel," Surmeier said. "By shutting down the channel, we should be able to slow the progression of the disease or significantly reduce the risk that anyone would get Parkinson’s disease if they take this drug early enough."
"We’ve developed a molecule that could be an entirely new mechanism for arresting Parkinson’s disease, rather than just treating the symptoms," Silverman said.
The compounds work in a similar way to the drug isradipine, for which a Phase 2 national clinical trial with Parkinson’s patients –- led by Northwestern Medicine neurologist Tanya Simuni, M.D. — was recently completed. But because isradipine interacts with other channels found in the walls of blood vessels, it can’t be used in a high enough concentration to be highly effective for Parkinson’s disease. (Simuni is the Arthur C. Nielsen Professor of Neurology at the Feinberg School and a physician at Northwestern Memorial Hospital.)
The challenge for Silverman was to design new compounds that specifically target this rare Cav1.3 channel, not those that are abundant in blood vessels. He and colleagues first used high-throughput screening to test 60,000 existing compounds, but none did the trick.
"We didn’t want to give up," Silverman said. He then tested some compounds he had developed in his lab for other neurodegenerative diseases. After Silverman identified one that had promise, Soosung Kang, a postdoctoral associate in Silverman’s lab, spent nine months refining the molecules until they were effective at shutting only the Cav1.3 channel.
In Surmeier’s lab, the drug developed by Silverman and Kang was tested by graduate student Gary Cooper in regions of a mouse brain that contained dopamine neurons. The drug did precisely what it was designed to do, without any obvious side effects.
"The drug relieved the stress on the cells," Surmeier said.
For the next step, the Northwestern team has to improve the pharmacology of the compounds to make them suitable for human use, test them on animals and move to a Phase 1 clinical trial.
"We have a long way to go before we are ready to give this drug, or a reasonable facsimile, to humans, but we are very encouraged," Surmeier said.
(Source: eurekalert.org)
Challenging Parkinson’s Dogma: Dopamine may not be the only key player in this tragic neurodegenerative disease
Scientists may have discovered why the standard treatment for Parkinson’s disease is often effective for only a limited period of time. Their research could lead to a better understanding of many brain disorders, from drug addiction to depression, that share certain signaling molecules involved in modulating brain activity.
A team led by Bernardo Sabatini, Takeda Professor of Neurobiology at Harvard Medical School, used mouse models to study dopamine neurons in the striatum, a region of the brain involved in both movement and learning. In people, these neurons release dopamine, a neurotransmitter that allows us to walk, speak and even type on a keyboard. When those cells die, as they do in Parkinson’s patients, so does the ability to easily initiate movement. Current Parkinson’s drugs are precursors of dopamine that are then converted into dopamine by cells in the brain.
The flip side of dopamine dearth is dopamine hyperactivity. Heroin, cocaine and amphetamines rev up or mimic dopamine neurons, ultimately reinforcing the learned reward of drug-taking. Other conditions such as obsessive-compulsive disorder, Tourette syndrome and even schizophrenia may also be related to the misregulation of dopamine.
In the October 11 issue of Nature, Sabatini and co-authors Nicolas Tritsch and Jun Ding reported that midbrain dopamine neurons release not only dopamine but also another neurotransmitter called GABA, which lowers neuronal activity. The previously unsuspected presence of GABA could explain why restoring only dopamine could cause initial improvements in Parkinson’s patients to eventually wane. And if GABA is made by the same cells that produce other neurotransmitters, such as depression-linked serotonin, similar single-focus treatments could be less successful for the same reason.
“If what we found in the mouse applies to the human, then dopamine’s only half the story,” said Sabatini.